Jiang, Haiying <br/><br/>
Cathepsin K-mediated Notch1 activation contributes to neovascularization in response to hypoxia.  [electronic resource] 

 -  Nature communications  Jun 2014 
 - 3838 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>2041-1723 
<br/><br/><label>Standard No.: </label>10.1038/ncomms4838  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Animals<br/>Basic Helix-Loop-Helix Transcription Factors--metabolism<br/>Capillaries--pathology<br/>Cathepsin K--genetics<br/>Cell Cycle Proteins--metabolism<br/>Femoral Artery--surgery<br/>Hindlimb--blood supply<br/>Homeodomain Proteins--metabolism<br/>Hypoxia--genetics<br/>Ischemia<br/>Laser-Doppler Flowmetry<br/>Ligation<br/>Mice<br/>Mice, Knockout<br/>Muscle, Skeletal--blood supply<br/>Neovascularization, Physiologic--genetics<br/>Phosphorylation<br/>Proto-Oncogene Proteins c-akt--metabolism<br/>RNA, Messenger--metabolism<br/>Receptor, Notch1--metabolism<br/>Repressor Proteins--metabolism<br/>Reverse Transcriptase Polymerase Chain Reaction<br/>Transcription Factor HES-1<br/>Vascular Endothelial Growth Factor A--metabolism<br/>Vascular Endothelial Growth Factor Receptor-1--metabolism